Killing arthritogenic fibroblast-like synoviocytes: an example using cytotoxic aptamers binding nucleolin. Editorial Article uri icon

Overview

abstract

  • "Pauci-immune" and "fibroblast-rich" synovial pathotypes are predictors of resistance to multi-drug immunosuppression. For these "difficult-to-treat" (D2T) endotypes of rheumatoid arthritis (RA), depletion of arthritogenic fibroblast-like synoviocytes (FLS) has emerged as promising treatment strategy. Profiling at a single-cell level has enabled the molecular characterization of distinct subpopulations of arthritogenic FLS. Advances in molecular engineering have empowered the development of multiple modalities (anti-FLS antibodies, T-cell engagers, cytotoxic cells with chimeric receptors recognizing FLS-specific antigens) to achieve depletion of arthritogenic subpopulations of FLS with unprecedented selectivity. A recently published study highlighted in this article, adds apoptosis-promoting aptamers in the armamentarium of the FLS-killing pipeline.

publication date

  • July 14, 2025

Research

keywords

  • Aptamers, Nucleotide
  • Arthritis, Rheumatoid
  • Fibroblasts
  • Phosphoproteins
  • RNA-Binding Proteins
  • Synoviocytes

Identity

PubMed Central ID

  • PMC12261783

Scopus Document Identifier

  • 105010689561

Digital Object Identifier (DOI)

  • 10.1186/s13075-025-03618-4

PubMed ID

  • 40660355

Additional Document Info

volume

  • 27

issue

  • 1